aaa综合征的一种新变异。

E. Demet Akbaş, Ö. Özalp Yüreğir, Ö. Anlaş, Z. Özçelik, O. Zerrin Tolunay
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引用次数: 0

摘要

aaa综合征是一种常染色体隐性遗传的多系统疾病,于1978年首次发现。aaa综合征具有较高的基因型和表型异质性,并与染色体12q13上鉴定的AAAS基因突变有关。男,14岁,以虚弱、肤色变黑4个月来门诊就诊。体格检查发现皮肤和粘膜色素沉着。晨间皮质醇1.8 μg/dL, ACTH >1250 ng/L。Schirmer试验显示无泪。患者食管镜检查发现粘膜苍白,贲门狭窄。分子遗传学分析证实AAAS基因为纯合突变c.1368_1372delGCTCA (p.Gln456HisfsTer38)所致的aaa综合征。这种变异被认为是一种可能的致病性,因为它会引起框架移位,从而改变蛋白质结构。通过对患者父母的遗传分析,在父母双方均检测到c.1368_1372delGCTCA突变的AAAS基因为杂合的。据我们所知,这是首次报道纯合突变:c.1368_1372delGCTCA (p.Gln456HisfsTer38)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A Novel Variant in Triple A Syndrome.
Triple A syndrome is an autosomal recessive inherited multisystem disorder that was first described in 1978. Triple A syndrome has a high genotypic and phenotypic heterogeneity and has been linked with mutations in the AAAS gene, which has been identified on chromosome 12q13. A 14 years old male patient applied to outpatient clinic complaining of weakness and darkening of skin color since 4 months. On physical examination hyperpigmentation was observed on both the skin and mucosa. The morning cortisol level was 1.8 μg/dL and ACTH was >1250 ng/L. Schirmer test showed absence of tears. In the patient's esophagoscopy, mucosal paleness and stenosis of the cardia were observed. Molecular genetic analysis of AAAS gene confirmed the diagnosis of triple A syndrome caused by homozygous mutation: c.1368_1372delGCTCA (p.Gln456HisfsTer38). This variant is considered to be a possible pathogenic because it causes a frame shift that changes the protein structure. As a result of the genetic analysis of the patient's parents, the AAAS gene was detected as heterozygous in both parents for the c.1368_1372delGCTCA mutation. To the best of our knowledge, this is the first report of homozygous mutation: c.1368_1372delGCTCA (p.Gln456HisfsTer38).
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